Author + information
- Received September 26, 1983
- Revision received December 2, 1983
- Accepted December 13, 1983
- Published online April 1, 1984.
- Gerald Maurer, MD, FACC,
- Marco A.R. Torres, MD,
- Eliot Corday, MD, FACCa,
- Roberto V. Haendchen, MD and
- Samuel Meerbaum, PhD, FACC
- ↵aAddress for reprints: Eliot Corday, MD, Cedars-Sinai Medical Center, Halper Research Building, 8700 Beverly Blvd., Los Angeles, California 90048.
Two-dimensional echocardiography during agitated saline contrast injections into the left ventricle was applied in eight closed chest dogs to examine the degree of mitral valve regurgitation encountered with pacing from two sites: 1) at the right ventricular apex and 2) within the coronary sinus at the base of the left ventricle. Pacing was at a rate of 10 beats/min above the sinus rate, and ranged from 60 to 120 beats/min. Hemodynamic variables were monitored, and data on global and regional left ventricular function were derived from a series of short- and long-axis cross-sectional echographic images. The degree of valvular regurgitation was assessed independently by two observers, and systolic appearance of echo contrast in the left atrium was graded as 0 to +4. Although no mitral regurgitation was noted in sinus rhythm, regurgitation was severe with right ventricular apical pacing (3.2 ± 0.7, mean ± standard deviation) and relatively mild (0.9 ± 0.7) with basal pacing (p < 0.01 and 0.05, respectively), Relative to sinus rhythm, thermodilution stroke volume was significantly (p < 0.05) depressed by both apical and basal pacing (from 32.6 ± 14.6 to 25.0 ± 7.9 and 26.0 ± 7.6 cc, respectively), but there was no significant difference between the two pacing sites. Mapping of regional function at six levels of the left ventricle revealed significant heterogeneities, with maximal dysfunction noted in the vicinity of the pacing site.
It is concluded that significant differences in mitral regurgitation exist depending on the site of pacing, with apical pacing causing severe regurgitation and abnormal regional contraction near the pacing site.
This study was supported in part by Grants HL 17651-09 and HL 14644-10 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; The Ahmanson Foundation, W. M. Keck Foundation, The Medallion Group, Mrs. Dorothy Forman, Mr. Tony Murray, Mrs. Doris Light, Mr. Morris Blank and Mr. J. C. Dunas, Los Angeles, California.
- Received September 26, 1983.
- Revision received December 2, 1983.
- Accepted December 13, 1983.
- American College of Cardiology Foundation